Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice

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Frequent consumption of a diet high in fat and sucrose contributes to lifestyle-related diseases. However, limited information is available regarding the short-term effects of such a diet on the onset of obesity-associated metabolic abnormalities. Methods Male C57BL/6 J mice were divided into two groups and fed a standard chow diet (control group) or a high fat–high sucrose diet containing 21% fat and 34% sucrose (HF–HS diet group) for 2 or 4 weeks. Results The HF–HS diet significantly induced body weight gain beginning at week 1 and similarly increased mesenteric white adipose tissue weight and plasma insulin levels at weeks 2 and 4. Plasma resistin levels were notably elevated after feeding with the HF–HS diet for 4 weeks. Measurement of hepatic triglycerides and Oil Red O staining clearly indicated increased hepatic lipid accumulation in response to the HF–HS diet as early as 2 weeks. Quantitative PCR analysis of liver and white adipose tissue indicated that, starting at week 2, the HF–HS diet upregulated mRNA expression from genes involved in lipid metabolism and inflammation and downregulated genes involved in insulin signalling. Although plasma cholesterol levels were also rapidly increased by the HF–HS diet, no differences were found between the control and HF–HS diet–fed animals in the expression of key genes involved in cholesterol biosynthesis. Conclusions Our study demonstrates that the rapid onset of hepatosteatosis, adipose tissue hypertrophy and hyperinsulinemia by ingestion of a diet high in fat and sucrose may possibly be due to the rapid response of lipogenic, insulin signalling and inflammatory genes.

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Publié le 01 janvier 2012
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Yanget al. Diabetology & Metabolic Syndrome2012,4:32 http://www.dmsjournal.com/content/4/1/32
DIABETOLOGY&METABOLIC SYNDROME
R E S E A R C HOpen Access Diet high in fat and sucrose induces rapid onset of obesityrelated metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice * ZhiHong Yang , Hiroko Miyahara, Jiro Takeo and Masashi Katayama
Abstract Background:Frequent consumption of a diet high in fat and sucrose contributes to lifestylerelated diseases. However, limited information is available regarding the shortterm effects of such a diet on the onset of obesity associated metabolic abnormalities. Methods:Male C57BL/6 J mice were divided into two groups and fed a standard chow diet (control group) or a high fathigh sucrose diet containing 21% fat and 34% sucrose (HFHS diet group) for 2 or 4 weeks. Results:The HFHS diet significantly induced body weight gain beginning at week 1 and similarly increased mesenteric white adipose tissue weight and plasma insulin levels at weeks 2 and 4. Plasma resistin levels were notably elevated after feeding with the HFHS diet for 4 weeks. Measurement of hepatic triglycerides and Oil Red O staining clearly indicated increased hepatic lipid accumulation in response to the HFHS diet as early as 2 weeks. Quantitative PCR analysis of liver and white adipose tissue indicated that, starting at week 2, the HFHS diet upregulated mRNA expression from genes involved in lipid metabolism and inflammation and downregulated genes involved in insulin signalling. Although plasma cholesterol levels were also rapidly increased by the HFHS diet, no differences were found between the control and HFHS dietfed animals in the expression of key genes involved in cholesterol biosynthesis. Conclusions:Our study demonstrates that the rapid onset of hepatosteatosis, adipose tissue hypertrophy and hyperinsulinemia by ingestion of a diet high in fat and sucrose may possibly be due to the rapid response of lipogenic, insulin signalling and inflammatory genes. Keywords:High fathigh sucrose diet, Hepatosteatosis, Insulin signalling, Inflammation
Background Being overweight or obese is one of the leading risks for death worldwide. Increasing evidence has indicated that obesity is linked to numerous comorbidity diseases such as type 2 diabetes, hypertension, hypercholesterolaemia, hypertriglyceridaemia, and nonalcoholic fatty liver dis ease [13]. It is estimated that 2025% of the worlds adult population has obesityrelated metabolic syndrome,
* Correspondence: yangzh@nissui.co.jp Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd., 323 Nanakuni 1 Chome Hachioji, Tokyo 1920991, Japan
and they are twice as likely to die and three times as likely to have a heart attack or stroke compared with people without the syndrome [4,5]. Besides an obeso genic environment and reduced energy expenditure dur ing work and leisure activities, one of the primary causes of the current epidemic of obesity and related metabolic disorders is related to the westernstyle diet, which includes excessive intake of highfat and highsucrose foods. Several studies have assessed the longterm (over 10 weeks~ 2years) effects of highfat and/or high sucrose diets on metabolic risk factors [68]. On the
© 2012 Yang et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.